Biology subjects

Vitipon, M.

Publications and source records attributed to Vitipon, M..

6 recordsLinked to original sources

bioRxiv2026

Effects of polystyrene and polylactide nanoparticles on macrophages under a repeated exposure mode

Micro and nanoplastics are pollutants which concentration in different biotopes increases continuously over time, which poses the question of their potential effects on health. In animals, these micro and nanoplastics are recognized as particulate materials and thus handled by macrophages, which are therefore a key cell type to study. Most studies have used an experimental scheme in which the cells are exposed to a single dose of plastics, with a readout made immediately after exposure. However, this classical experimental scheme does not take into account the impact of biopersistence, nor the potential cellular adaptation that may take place when cells are exposed repeatedly to a low dose of plastics. We thus used a repeated exposure scheme, in order to better take into account these phenomena. Within this frame, we compared the macrophages responses to a persistent nanoplastic, i.e. polystyrene nanoparticles and to a biodegradable nanoplastic, i.e. polylactide, by a combination of proteomic and targeted experiments. Our results show that under this repeated exposure scheme, the proteome changes were of a lesser (for PS) or similar (for PLA) extent than under the acute exposure mode, indicating cell adaptation. However, PLA particles induced mitochondrial dysfunction and depression of response to bacterial molecules perceived as danger signals, such as lipopolysaccharide. Polystyrene nanoparticles also induced a slight alteration of the immune functions of macrophages. This indicates harmful effects even in the repeated exposure scheme.

pharmacology and toxicology↗

bioRxiv2025

Effects of manganese dioxide on macrophages under different exposure schemes

Manganese dioxide is a material that is more and more used in its particular form, for many industrial applications such as chemical catalysis or for batteries. Thus, workers can be exposed to this particulate chemical. It is known that overexposure to manganese leads to a brain disease called manganism. However, manganese is also known to impact the pulmonary function, which is important as pulmonary exposure is of prime importance for workers. We thus investigated the effects of manganese dioxide on macrophages, i.e. the scavenger cells that take particulates in charge in our bodies. To this purpose, we used a combination of proteomic and targeted approaches, in order to obtain a wide view of the cellular responses to manganese dioxide. We also used a repeated exposure mode, in order to better mimic occupational exposure. Our results point out the fact that manganese oxide nanoparticles are rather toxic for macrophages and induce mitochondrial dysfunction, oxidative stress and a pro-inflammatory response. Environmental significanceManganese dioxide is more and more used in batteries, so that workers in batteries factories are exposed to this metallic oxide. As always for particulate materials, macrophages are the first line of defense of the organism. We thus investigated the effects of manganese dioxide on macrophages, using a repeated exposure scheme to mimic occupational exposure, and the effects were documented by a combination of proteomic and targeted approaches. The functional effects include mitochondrial dysfunction, oxidative stress and inflammation.

pharmacology and toxicology↗

bioRxiv2025

The devil lies in the details: small structural and chemical changes in iron oxide pigments largely alter the biological outcomes in macrophages

Because of their technical qualities, such as resistance to fading and to high temperatures, mineral pigments are still widely used nowadays. Among the diversity of mineral pigments, iron oxide pigments represent a widely-used class, because of their technical qualities, diversity of shades (from yellow to red to brown to black) and low toxicity compared to heavy metals-based pigments. However, a low toxicity does not mean the absence of adverse effects. We thus investigated the effects on macrophages of two different subtypes of Pigment Red 101, i.e. hematite, produced by two different processes, namely a wet precipitation process and a calcination process. Macrophages were chosen as a target cell type because they represent the main scavenger cell type that is in charge of handling particulate materials in the body. During this comparison, we realized that the calcined pigment was contaminated from the start by bacterial endotoxins, which induced intense inflammatory responses and biased the comparison. After depyrogenation, the calcined pigment proved to dissolve to a higher extent in macrophages, but to show less important adverse effects (e.g. alteration of the mitochondrial transmembrane potential, oxidative stress and inflammatory responses) than the precipitated pigment in a recovery exposure mode, allowing to investigate delayed effects of the pigments. Thus, despite their identical pigment number, pigments differing in their structure and in their synthesis induce different responses from living cells, even if administrated in equivalent amount. This should be taken into account for some applications, such as tattooing. Moreover, endotoxin contamination should also be checked to increase workers and users safety

pharmacology and toxicology↗

bioRxiv2025

Beyond the ink: cellular and molecular effects of iron-based pigments on macrophages

As ochre, iron oxide is among the most ancient pigments used by mankind for different purposes, including tattooing as demonstrated on tattoed mummies. Iron oxides are still used in tattooing nowadays and especially in dermopigmentation, an area of medical tattoing aiming at restoring the color of skin. This ancient use of iron oxide does not mean that it has no effect on cells, and especially on macrophages, the cells that maintain pigments particles on site in tattoos. We thus investigated in vitro the delayed/sustained effects of iron oxide pigments on macrophages, i.e. the effects occurring a few days after the exposure to pigments, on pigments-loaded macrophages but in a pigment-free medium, mimicking the status of tattooed skin after all the pigment particles have been captured. By combining proteomic and targeted approaches, we determined that red iron oxide (but not black iron oxide) induces perturbations in mitochondria, altering the mitochondrial transmembrane potential. Red iron oxide also induces oxidative stress and the secretion of pro-inflammatory cytokines such as interleukin 6 and tumor necrosis factor. Thus, red iron oxide induces adverse effects on macrophages that may persist over time, owing to its low intracellular dissolution.

immunology↗

bioRxiv2024

The VVBlue assay: a plate-readable, dye exclusion-based cell viability assay for the toxicological testing of chemicals

A viability test for in vitro cultures, based on the intake of the textile dye Alphazurine A by dead cells and its exclusion by viable cells, is described. This test uses the affinity of Alphazurine A for proteins, so that the dye is retained in dead cells even after rinsing, while its anionic character prevents it from entering live cells. This feature makes this dye exclusion test amenable to a reading in a plate format. The Alphazurine viability test provides an indicator of the absolute number of dead cells present in the culture well. To reach a cell viability index, a "dead cells" control (e.g. cells killed with ethanol) must be added. We also describe a double viability test, which first uses the Alphazurine assay to provide the number of dead cells then a crystal violet assay to provide an index of the number of cells present in the plate. This double test provides a complete appraisal of the situation in the cell culture wells, and has been compared to other viability tests such as propidium iodide exclusion or tetrazolium reduction. Its performances to study the toxicity of substances such as pigments are also established, and allowed us to publish the first public toxicological data on the recently described Pigment Blue 86.

cell biology↗

bioRxiv2024

Biobased, Biodegradable but not bio-neutral: about the effects of polylactic acid nanoparticles on macrophages

Plastics are persistent pollutants, because of their slow degradation, which suggests that they may lead to cumulative and/or delayed adverse effects due to their progressive accumulation over time. Macroplastics produced by human activity are released in the environment, where they degrade into micro and nanoplastics that are very easily uptaken by a wide variety of organisms, including humans. Microplastics and nanoplastics being particulates, they are handled in the body by specialized cells such as macrophages (or their evolutionary counterparts), where they can elicit a variety of responses. One solution to alleviate the problems due to biopersistence, such as accumulation over life, would be to use biodegradable plastics. One of the emerging biodegradable plastics being polylactide, we decided to test the responses of macrophages to polylactide nanoparticles, using a combination of untargeted proteomics and targeted validation experiments. Proteomics showed important adaptive changes in the proteome in response to exposure to polylactide nanoparticles. These changes affected for example mitochondrial, cytoskeletal and lysosomal proteins, but also proteins implicated in immune functions or redox homeostasis. Validation experiments showed that many of these changes were homeostatic, with no induced oxidative stress and no gross perturbation of the mitochondrial function. However, polylactide particles altered the immune functions such as phagocytosis (-20%) or cytokine production (2-fold increase for TNF production), which may translate into a decreased ability to macrophages to respond to bacterial infections. Furthermore, polylactide particles also induced moderate cross-toxicity with some quinones such as phenanthrene quinone, a combustion by-product that is a suspected carcinogen.

pharmacology and toxicology↗